Sunitinib Malate

Licensed by Pfizer Catalog No.S1042

Sunitinib Malate Chemical Structure

Molecular Weight(MW): 532.56

Sunitinib Malate is a multi-targeted RTK inhibitor targeting VEGFR2 (Flk-1) and PDGFRβ with IC50 of 80 nM and 2 nM in cell-free assays, and also inhibits c-Kit.

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In DMSO USD 191 In stock
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USD 147 In stock
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Cited by 42 Publications

12 Customer Reviews

  • PDGF-AA induces Ezh2 expression and proliferation in juvenile islets but not in adult islets. Western immunoblots of indicated islet proteins from 3 week or 9 month-old WT islets 2 days after exposure to PDGF-AA alone, or PDGF-AA plus RTK inhibitors Sunitinib.

    Nature 2011 478(7369):349-55. Sunitinib Malate purchased from Selleck.

    Assessment of effects on human juvenile or adult islets after exposure to PDGF-AA (50 ng/ml) for 2 days, with or without Sunitinib (2 uM) or U0126 (10 uM)co-treatment. Average percentage of BrdU+ insulin+ cells was morphometry from sectioned islets immunostained for insulin (green), glucagon (white) and BrdU (red). n = 3-6 independent experiments.

    Nature 2011 478(7369):349-55. Sunitinib Malate purchased from Selleck.

  • Combinational treatment of kinase inhibitors induces the similar phenotype produced by PP1. All images are lateral view with dorsal to the top and anterior to the left. The combinational treatment of Dasatinib (D) or U0126 (U) with Sunitinib (SU),PTK787 (PTK), or ZM323881 (Z) resulted in the shrinkage of dorsal aorta.

    Cell Res 2011 21, 1080-1087. Sunitinib Malate purchased from Selleck.

    A, Tumor growth curves from the initial sunitinib drug trials, with endpoint set at 1,300 mm3 (mean ± SEM). Measurements began one week after tumor inoculation and on the day sunitinib treatment began. Subsequent experimental endpoints were set on the basis of these growth curves and their intersections with this data are shown. B, Histogram plot showing the distribution of tumor sizes at day 8 of treatment. Sunitinib-treated tumors exceeding 250 mm3 in size were identified as falling into the nonresponsive cohort. Sunitinib treatment significantly retards growth of responsive tumors.

    Cancer Res, 2017, 77(4):1008-1020 . Sunitinib Malate purchased from Selleck.

  • Sunitinib decreases FLT-3 and RET phosphor ylation but increases ERK phosphorylation in a time-dependent manner. H295R and SW13 cells were treated with sunitinib (10 nM) for various time points as indi-cated. Cell lysates were prepared and phospho-FLT-3, RET, and ERK levels were monitored by Western Blot-ting. Re-probing against FLT-3, RET, and ERK was done to ensure equal protein loading.

    Surgery 2012 152, 1045-50. Sunitinib Malate purchased from Selleck.

    Sunitinib or PD98059 decreases cell proliferation in a dose-dependent manner. H295R and SW13 cells were treated with various concentration of sunitinib or PD98059 for 48 hours as indicated. Treated cells were subjected to the MTS proliferation assay. Similar experiments were repeated 3 times. Histograms represent relative % of OD490 nm absorbance (* P < .05). All data are relative multiples of expression compared with untreated cells. The data are representative of three experiments and are expressed as the mean ?SE.

    Surgery 2012 152, 1045-50. Sunitinib Malate purchased from Selleck.

  • Autophagic activation in sunitinib- and sorafenib- but not AZD6244-treated cells. Medullary thyroid cancer-1.1 (MTC-1.1; A) and TT ( B) cells were treated with dimethyl sulfoxide (DMSO), sunitinib (50 nM), sorafenib (10 nM), AZD6244 (30 nM), or everolimus (20 nM) for 48 hours. Cell lysates were prepared, and light chain 3 (LC3)-I and -II cleaved caspase-3 protein levels were monitored by Western blotting. Reprobing against actin was per formed to ensure equal protein loading. ( C ) MTC-1.1 and TT cells were transiently transfected with autophagy protein 5 (Atg-5) small inter fering RNA. Transfection with scrambled small inter fering RNA was used as a control. After transfection, cells with and without Atg-5 knockdown were exposed to DMSO or 20 nM of everolimus for 48 hours. Cell lysates were pre- pared and LC3-I and -II protein expression levels were monitored by Western blotting. Reprobing against Atg-5 was per formed to monitor Atg-5 knockdown efficiency. Reprobing against actin was per formed to ensure equal protein.

    Surgery 2012 152, 1142-9. Sunitinib Malate purchased from Selleck.

    Autophagy inhibition blocks the antiproliferative effects of sunitinib and sorafenib but not AZD6244. Medullary thyroid cancer–1.1 (MTC-1.1) and TT cells were transfected transiently with scrambled or autophagy protein 5 (Atg-5) small inter fering RNA. After transfection, cells with and without Atg-5 knockdown were exposed to sunitinib (50 nM), sorafenib (10 nM), and AZD6244 (30 nM) for 48 hours. Treated cells were subjected to a 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium proliferation assay. Similar experiments were repeated 3 times. Histograms represent the relative percent of OD490 nM absorbance. The asterisk indicates significance versus scrambled small inter fering RNA–treated control ( P < .05). All data are relative multiples of expression compared to untreated cells. The data are representative of 3 experiments and are expressed as the mean ± the standard error.

    Surgery 2012 152, 1142-9. Sunitinib Malate purchased from Selleck.

  • Sunitinib limits the colonial growth of HT-29 by downregulating HIF-1a. (A) The number and size of colonies formed in soft agar. The numbers of small colonies (<50 μm diameter) were not different among conditions of a serial concentration of sunitinib. On the contrary, large colonies (>50 μm diameter) disappeared after incubation with sunitinib. Each point represents the mean and SD from four separate experiments. (B) HIF-1a expression and hypoxia within HT-29 colony. After colonies grew for 4 weeks, HIF-1a and hypoxia were visualized by immunofluoroscence staining. Bar = 20 μm.

    Biochem Bioph Res Co 2010 398, 205–211. Sunitinib Malate purchased from Selleck.

    2. Sunitinib downregulates HIF-1a. (A) Dose-dependent repression of HIF-1a protein level by sunitinib in HT-29. HT-29 cells were incubated under normoxic (N) or hypoxic (H) conditions in the presence of sunitinib for 24 h. HIF-1a and ARNT proteins in total cell lysates were analyzed by Western blotting. (B) Sunitinib attenuates the hypoxic induction of HIF-1 target genes. RNAs were isolated from HT-29 cells subjected to normoxia (N) or hypoxia (H) in the presence of sunitinib for 16 h. The mRNAs of HIF-1a and its target genes were analyzed by RT-PCR and autoradiography. PGK1 indicates phosphoglycerate kinase 1; PDK1, pyruvate dyhydrogenase kinase 1; CAIX, carbonic anhydrase IX. (C) Sunitinib-induced HIF-1 inhibition. Epo-enhancer and b- galactosidase reporter plasmids were co-transfected into HEK293 cells. After 16 h incubation, luciferase and b-galactosidase activities were measured. *P < .05 versus the hypoxic control.

     

     

    Biochem Bioph Res Co 2010 398, 205–211. Sunitinib Malate purchased from Selleck.

  • Sunitinib inhibits 50-UTR-dependent translation of HIF-1a. (A) 50 cap-dependent translational activity of HIF-1a. The luciferase reporter plasmid contains the HIF-1a 50-UTR segment between the tk promoter and the luciferase gene. HT-29 cells were co-transfected with the reporter plasmid (8 lg per 100-mm dish) and the b-gal plasmid (4 μg). After 16 h incubation under normoxic or hypoxic conditions with sunitinib, cells were lysed and subjected to luciferase assay. *P < .05 versus the hypoxic control. (B) IRES-dependent translational activity of HIF-1a. The luciferase reporter plasmid contains the HIF-1a 50-UTR segment between the GFP gene and the luciferase gene. HT-29 cells were co-transfected with the reporter plasmid (8 μg) and the b-gal plasmid (4 μg). *P < .05 versus the hypoxic control. (C) Sunitinib inhibits phosphorylation of Akt. After 8 h incubation under hypoxic condition with sunitinib, HT-29 cells were lysed and subjected to Western blotting. (D) Sunitinib suppresses HIF-1a in VHL-null RCC4 cells. VHL (-/-) RCC4 cells were incubated under normoxic conditions sunitinib for 8 h, and HIF-1a in total cell lysates was analyzed by Western blotting.

     

     

    Biochem Bioph Res Co 2010 398, 205–211. Sunitinib Malate purchased from Selleck.

    Experimental layout for VEGF signaling blocking and LCMV infection in WT mice. Mice received two injections on day 0 and 3 p.i. of Abs as described in Material and Methods, or daily gavage of the VEGFR/PDGFR-inhibitor sunitinib. Inguinal LN volume on day 0 (D0) or day 8 (D8) p.i. after treatment of mice with control Ig or anti-VEGFR2, anti-VEGF-A Abs or sunitinib. Pooled from 1-2 independent experiments with 3-5 mice per treatment. D. Total HEV length on day 0 (D0) or day 8 (D8) p.i. as in C. No significant difference was found in C and D between day 8 control Ig and Ab- or inhibitor-treated values (One-way ANOVA).

    AACR Sunitinib Malate purchased from Selleck.

Purity & Quality Control

Choose Selective PDGFR Inhibitors

Biological Activity

Description Sunitinib Malate is a multi-targeted RTK inhibitor targeting VEGFR2 (Flk-1) and PDGFRβ with IC50 of 80 nM and 2 nM in cell-free assays, and also inhibits c-Kit.
Targets
Kit [1]
(Cell-free assay)
FLT3 [1]
(Cell-free assay)
PDGFRβ [1]
(Cell-free assay)
VEGFR2 [1]
(Cell-free assay)
2 nM 80 nM
In vitro

Sunitinib also potently inhibits Kit and FLT-3. [1] Sunitinib is a potent ATP-competitive inhibitor of VEGFR2 (Flk1) and PDGFRβ with Ki of 9 nM and 8 nM, respectively, displaying >10-fold higher selectivity for VEGFR2 and PDGFR than FGFR-1, EGFR, Cdk2, Met, IGFR-1, Abl, and src. In serum-starved NIH-3T3 cells expressing VEGFR2 or PDGFRβ, Sunitinib inhibits VEGF-dependent VEGFR2 phosphorylation and PDGF-dependent PDGFRβ phosphorylation with IC50 of 10 nM and 10 nM, respectively. Sunitinib inhibits VEGF-induced proliferation of serum-starved HUVECs with IC50 of 40 nM, and inhibits PDGF-induced proliferation of NIH-3T3 cells overexpressing PDGFRβ or PDGFRα with IC50 of 39 nM and 69 nM, respectively. [2] Sunitinib inhibits phosphorylation of wild-type FLT3, FLT3-ITD, and FLT3-Asp835 with IC50 of 250 nM, 50 nM, and 30 nM, respectively. Sunitinib inhibits the proliferation of MV4;11 and OC1-AML5 cells with IC50 of 8 nM and 14 nM, respectively, and induces apoptosis in a dose-dependent manner. [3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
3T3 NYDEPYpRU2mwYYPlJGF{e2G7 NH\jbJZKdmirYnn0bY9vKG:oIGDES2YucW6mdXPl[EBDemSXIHnuZ49zeG:{YYTpc44hf2m2aDDJR|UxKG:oIECuNFA4KM7:TR?= NHn3TpcyOjZ2NkCxPS=>
3T3 MmPuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUXJcohq[mm2aX;uJI9nKFCuYYTlcIV1NWSncnn2[YQh\3Kxd4ToJIZi[3SxcjDpcoR2[2WmIEPUN{Bk\WyuIIDyc4xq\mW{YYTpc44hf2m2aDDJR|UxKG:oIECuNFEh|ryP MnfoNVI3PDZyMUm=
3T3 M1TpRmZ2dmO2aX;uJGF{e2G7 M2DQWGlvcGmkaYTpc44hd2ZiVnHzZ5Vt[XJiZX7kc5Rp\WyrYXyg[5Jwf3SqIH\hZ5RweiC{ZXPldJRweiC5aYToJGlEPTBib3[gNE4xPSEQvF2= MmjZNVI3PDZyMUm=
3T3 MVjLbY5ie2ViQYPzZZk> MXOyNEBucW5? MYjEUXNQ MkSwR4VtdHWuYYKgbY5pcWKrdHnvckBw\iCYRVfGJIlv\HWlZXSgbJVu[W5iS1TSJJBpd3OyaH;yfYxifGmxbjD3bZRpKEmFNUCgc4YhOC5yMkKg{txO M2\5VVE3OTZ{MEC4
NIH3T3 NEm0TopMcW6jc3WgRZN{[Xl? NIHs[oszOCCvaX6= MlyzSG1UVw>? NIDXSItqdmirYnn0JIh2dWGwIFvEVkBscW6jc3Wg[ZhxemW|c3XkJJdqfGhiSVO1NEBw\iByLkCxPEDPxE1? NXvTSYFOOTZzNkKwNFg>
A549 NHHSe41HfW6ldHnvckBCe3OjeR?= MXXEUXNQ MVrJcohq[mm2aX;uJI9nKGNvTXX0JIRmeGWwZHXueEBJT0ZvaX7keYNm\CCqdX3hckBCPTR7IHPlcIwhdWmpcnH0bY9vKHerdHigTWM2OCCxZjCyJO69VQ>? M3jXclE5PDN2MUS1
DU145 NV3mXVR7TnWwY4Tpc44hSXO|YYm= NWrVN3JiTE2VTx?= MYXJcohq[mm2aX;uJI9nKGNvTXX0JIRmeGWwZHXueEBJT0ZvaX7keYNm\CCqdX3hckBFXTF2NTDj[YxtKHOlYYT0[ZJqdmdid3n0bEBKSzVyIH;mJFExKM7:TR?= M4fFSFE5PDN2MUS1
KB3-1 M{XlWGN6fG:2b4jpZ{BCe3OjeR?= NUjZWJlkPzJiaB?= NGrJOYNFVVOR M3TGU2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJHAu\3BvbnXnZZRqfmViS1KtN{0yKGOnbHzzJJdqfGhiSVO1NEBw\iB{LkOg{txO M1zCO|E6Ozl5M{Ky
KBV1 MkTWR5l1d3SxeHnjJGF{e2G7 NXjXSnpXPzJiaB?= NUTKT45qTE2VTx?= NFLMS3dEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBRNWeueXPvdJJwfGWrbj3lfJBz\XO|aX7nJGtDXjFiY3XscJMhf2m2aDDJR|UxKG:oIESuNUDPxE1? MlTCNVk{QTd|MkK=
A375 M3L2UGN6fG:2b4jpZ{BCe3OjeR?= MVu3NkBp MofSSG1UVw>? NULsNG5HUUN3ME21MlQh|ryP MXKxPVY2PDRyOB?=
RS4-11 MXvGeY5kfGmxbjDBd5NigQ>? MmTMNkBp MV7Jcohq[mm2aX;uJI9nKE[OVEOgZZV1d3Cqb4PwbI9zgWyjdHnvckB4cXSqIFnDOVAhd2ZiMD6wNFk6KM7:TR?= M{eyZVE6PjV2NEC4
RS4-11 MofNSpVv[3Srb36gRZN{[Xl? NXG0VHh1OiCq M{Kx[mlvcGmkaYTpc44hd2ZiRlzUN{BKXERibYX0ZY51KGG3dH;wbI9{eGixconsZZRqd25id3n0bEBKSzVyIH;mJFAvODN2IN88US=> MXixPVY2PDRyOB?=
Sf9 NHnoWWNMcW6jc3WgRZN{[Xl? MVGzNEBucW5? Ml;wTY5pcWKrdHnvckBw\iCJU2SteIFo\2WmIG\FS2ZTKGW6cILld5Nm\CC5aYToJGlEPTBib3[gNE4yQDVizszN Mn;sNVk5PTRyNUG=
Ba/F3 NYLNflJnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlO4O|IhcA>? MnXOTWM2OD1zLkKg{txO M3q3OlIxOTF5MEC0
BaPTC2 NWP6SYN4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWS3NkBp M1LK[GlEPTB;MD6yNkDPxE1? Mn3MNlAyOTdyMES=
Sf9 MW\GeY5kfGmxbjDBd5NigQ>? NUDiT|h6OSCq MnfGSG1UVw>? NEjwOoRKdmirYnn0bY9vKG:oIHj1cYFvKHKnY3;tZolv[W62IFjpd{11[WepZXSgVmVVKGW6cILld5Nm\CC5aYToJGlEPTBib3[gNU4{KM7:TR?= NIO5e5QzODFzN{CwOC=>
H4 MmPNR5l1d3SxeHnjJGF{e2G7 NELrPZIyOCEQvF2= NEjtTHFVd3irY3n0fUBqdiCqdX3hckBJPCClZXzsdy=> M4PDZlIxOzVyOEC2
SF-539 NETmbpVMcW6jc3WgRZN{[Xl? NG[1U4M{OzNizszN M176N|YxKG2rbh?= M1jIT2ROW09? NF[3cm1KdmirYnn0bY9vKG:oIGDES2ZT[mW2YTDwbI9{eGixconsZZRqd25id3n0bEBKSzVyIH;mJFEzNjJizszN M1\vUVIxPDB|N{Cw
U251 NHWxdpFMcW6jc3WgRZN{[Xl? MlP3N|M{KM7:TR?= NHLOS5g3OCCvaX6= MX7EUXNQ NHG2fYJKdmirYnn0bY9vKG:oIG\FS2ZTOiCyaH;zdIhwenmuYYTpc44hf2m2aDDJR|UxKG:oIEG4Mlkh|ryP NIW2[oEzODRyM{ewNC=>
A431 NH\jZ|NMcW6jc3WgRZN{[Xl? MnXyTY5pcWKrdHnvckBw\iCSRFfGVoJmfGFiZYjwdoV{e2WmIIfpeIghUUN3MDDv[kAyOi5{IN88US=> NFriRZUzODV3OEC3Ni=>
A431 MWLLbY5ie2ViQYPzZZk> NGXSNFZKdmirYnn0bY9vKG:oIG\FS2ZTOiCneIDy[ZN{\WRid3n0bEBKSzVyIH;mJFE5NjlizszN MYeyNFU2QDB5Mh?=
HepG2 MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX[3NkBp NGeyeo1KSzVyPUOuPFEh|ryP M1LKS|IxPTdyNUK2
Kasumi-1 NYq4Sms4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MUe3NkBp NXOxWoh3UUN3ME2wMlAyPiEQvF2= NWW2OpMyOjB3N{C1NlY>
RS4-11 MV;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYG0TlBpPzJiaB?= Mk[yTWM2OD1zIN88US=> M4W1fVIxPTdyNUK2
THP1 NI\aS41Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3O3TFczKGh? M3v6dGlEPTB;MD61JO69VQ>? NYexPXNMOjB3N{C1NlY>
Kasumi-1 NFnCcXhHfW6ldHnvckBCe3OjeR?= M1XPR2lvcGmkaYTpc44hd2ZiYz3LbZQh[XW2b4Doc5NxcG:{eXzheIlwdiC5aYToJGlEPTBib3[gNE4xOTVizszN NFvJWlUzODh|M{CzPS=>
A549 NG\U[m5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYSxOkBp MX;BcpRqfHWvb4KgZYN1cX[rdImgZYdicW6|dDDoeY1idiCDNUS5JINmdGy| M2nqW|IyPDVyNE[z
HL60 MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NV30epZoOTZiaB?= NYnYZ49SSW62aYT1cY9zKGGldHn2bZR6KGGpYXnud5QhcHWvYX6gTGw3OCClZXzsdy=> MYSyNVQ2ODR4Mx?=
HUVEC MlfNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkfuNVYhcA>? MVvJcohq[mm2aX;uJI9nKF[HR1[tbY5lfWOnZDDj[YxtKHC{b3zp[oVz[XSrb36ge4l1cCCLQ{WwJI9nKDJwN{Wg{txO Mny2NlE1PTB2NkO=
HUVEC MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWSxOkBp NHjZO2hKdmirYnn0bY9vKG:oIHLGS2YucW6mdXPl[EBk\WyuIIDyc4xq\mW{YYTpc44hf2m2aDDJR|UxKG:oIESuNFQh|ryP MWSyNVQ2ODR4Mx?=
IM9 MkjNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYXBN3VKOTZiaB?= M{H2O2FvfGm2dX3vdkBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFnNPUBk\Wyucx?= NGGxTHozOTR3MES2Ny=>
K562 NETyZlBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{\iclE3KGh? M{XrfGFvfGm2dX3vdkBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFu1OlIh[2WubIO= Mn;mNlE1PTB2NkO=
MDA-MB-231 MmPnS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWP0bFV1OTZiaB?= NVywRmdDSW62aYT1cY9zKGGldHn2bZR6KGGpYXnud5QhcHWvYX6gUWRCNU2ELUKzNUBk\Wyucx?= MkLINlE1PTB2NkO=
H460 MnvhR5l1d3SxeHnjJGF{e2G7 MVm3NkBp MW\JR|UxRTJwNzFOwG0> MX6yNVYzOTh6MB?=
SMMC7721 NWX3Z2F3S3m2b4TvfIlkKEG|c3H5 NF63bWk4OiCq M4H1PGlEPTB;Nj60O{DPxE1? M3XpblIyPjJzOEiw
WI38 MnrSR5l1d3SxeHnjJGF{e2G7 MkLzO|IhcA>? M2nMdmlEPTB;OD61OkDPxE1? M2nUb|IyPjJzOEiw
HEK293 MmPET4lv[XOnIFHzd4F6 MnLjNVAxKG6P MV:xJIg> M4[2NoRw\XNibn;0JIlvcGmkaYSgWmVITi2rbnT1Z4VlKGG3dH;wbI9{eGixconsZZRqd25ib3[geJlzd3OrbnWgNVE4PSC{ZYPp[JVmKG:wIG\FS2ZTOiCneIDy[ZN{\WRiaX6gTGVMOjl|IHPlcIx{ MYOyNVg5PTJ6Nx?=
HUVEC MmjsSpVv[3Srb36gRZN{[Xl? M2SzRVEh|ryP MljGNlQhcA>? MnvTRY51cWGwZ3nv[4VvcWNiYXP0bZZqfHliYYPz[ZN{\WRiYYOg[IVkemWjc3WgbY4hXkWJRj3pcoR2[2WmIHPlcIwhdWmpcnH0bY9v M2npflIyQTZ|M{C1
HUVEC MnzjSpVv[3Srb36gRZN{[Xl? NHnOXHgyKM7:TR?= NX7pTHRXOSCq NWXTR2NxUW6qaXLpeIlwdiCxZjDFVmsheGixc4Doc5J6dGG2aX;uJIF1KFSqckKwNk9VgXJ{MESgbY4hXkWJRj3zeIlufWyjdHXkJGhWXkWF NFXZZoMzOTl4M{OwOS=>
HUVEC MmnJSpVv[3Srb36gRZN{[Xl? NUDtUWVOOSEQvF2= NH7kPFcyKGh? NGDnSopKdmirYnn0bY9vKG:oIHXOU3MheGixc4Doc5J6dGG2aX;uJIF1KFOncj2xNVczKGmwIG\FS2Yue3SrbYXsZZRm\CCKVW\FRy=> MkLsNlE6PjN|MEW=
HUVEC NX2zUItzU2mwYYPlJGF{e2G7 MYqxJO69VQ>? NUntSZNJOSCq M1PrU2lvcGmkaYTpc44hd2ZiVlXHSnIzKHCqb4PwbI9zgWyjdHnvckBifCC2eYKtNVE4PSCrbjDWSWdHNXO2aX31cIF1\WRiSGXWSWM> NGS5bIUzOTl4M{OwOS=>
HUVEC MUPGeY5kfGmxbjDBd5NigQ>? MmHONUDPxE1? NVLxdmdMOSCq MVLkc4V{KG6xdDDpcohq[mm2IFHLWEBxcG:|cHjvdplt[XSrb36gZZQhW2W{LUS3N{BqdiCYRVfGMZN1cW23bHH0[YQhUFWYRVO= NHjLd3EzOTl4M{OwOS=>
HL60 Mkj5R5l1d3SxeHnjJGF{e2G7 Mli3OVAh|ryP NIi2VGc1QCCq NIOwWlFFVVOR NIXaV2RKSzVyPUG1MlUh|ryP NEjTWHUzOjBzOUG4PC=>
K562 MUXDfZRwfG:6aXOgRZN{[Xl? NX;kOoZtPTBizszN NVXKbog4PDhiaB?= MXzEUXNQ NHWx[mpKSzVyPUKxMlkh|ryP Mn3ENlIxOTlzOEi=
PC3 MVnDfZRwfG:6aXOgRZN{[Xl? NXvrNZlYPTBizszN M4jRflQ5KGh? NFzORmJFVVOR M1rmRWlEPTB;MkWuNUDPxE1? M4fBOFIzODF7MUi4
SF-539 M1y0OGtqdmG|ZTDBd5NigQ>? M3XKV|M{OyEQvF2= M1nvOFYxKG2rbh?= M2LXXmlvcGmkaYTpc44hd2ZiUFTHSnJj\XSjIIT5do9{cW6nIHvpcoF{\SCjY4Tpeol1gSCrbjDQSGdHNUKELYP0bY12dGG2ZXSgbJVu[W5iU1[tOVM6KGOnbHzzJJdqfGhiSVO1NEBw\iBzMj6yJO69VQ>? MnryNlIzODR5NEG=
HAEC MonjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXqxNFAh|ryP NYHG[YJbPzJiaB?= NYLmZWV7SW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDIRWVEKGOnbHzzJIV5eHKnc4PpcochXkWJRmKge4l1cCCLQ{WwJI9nKDBwMTFOwG0> NFfTPGczOjR2NE[3PS=>
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NKM-1 M{f1SWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn;HTWM2OD17OD61NkBvVQ>? M{ez[nNCVkeHUh?=
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TE-15 NEPWNpdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mk\hTWM2OD13MEeuOlEhdk1? NIDnSYJUSU6JRWK=
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TE-8 MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MV3JR|UxRTJwM{ewN|gh|ryP M4W2[nNCVkeHUh?=
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KGN MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NE\TWo9KSzVyPUKuOlA{OzlizszN MoTMV2FPT0WU
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LAMA-84 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXXJR|UxRTJwNkm1OFUh|ryP NHnvTVJUSU6JRWK=
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SK-N-FI MVXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVvUT29{UUN3ME2xO{43QTF|IN88US=> M3zpd3NCVkeHUh?=
NTERA-S-cl-D1 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn\kTWM2OD1zNz64OVczKM7:TR?= NXflfFhIW0GQR1XS
NCI-H1882 MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml6zTWM2OD1zNz65PFM1KM7:TR?= MkDJV2FPT0WU
A704 MlTlS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXTJR|UxRTF5Lkm5NFQh|ryP MWXTRW5ITVJ?
L-428 NXPKcndjT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mnr4TWM2OD1zOD6wNVUyKM7:TR?= MV;TRW5ITVJ?
HCC1187 MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX7JR|UxRTF6LkCxPFch|ryP MXnTRW5ITVJ?
NCI-H1581 MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{H5NWlEPTB;MUiuNFg3PiEQvF2= M1z4U3NCVkeHUh?=
BB65-RCC NWq3SnMxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml;GTWM2OD1zOD60NVYzKM7:TR?= NWDqOG5MW0GQR1XS
EM-2 NEDWUJNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWHJR|UxRTF6LkW2O|Ih|ryP NF3XSoVUSU6JRWK=
Raji Mn3wS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHPx[I1KSzVyPUG5Mlk2PjVizszN M4XxO3NCVkeHUh?=
TE-1 NHLoU|VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlfjTWM2OD1{MD60NVA1KM7:TR?= NYDGOI1FW0GQR1XS
SW962 M2rz[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFzVZWlKSzVyPUKwMlQzQTNizszN NF65fFNUSU6JRWK=
MHH-NB-11 MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmfYTWM2OD1{MD61OVIyKM7:TR?= NXLEUnl{W0GQR1XS
no-10 M4W4bmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFq2NmVKSzVyPUKxMlAzPjRizszN NUm4Uoo1W0GQR1XS
GDM-1 NGHPNlNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGnxcI5KSzVyPUKxMlk1OTRizszN NVfUWVl2W0GQR1XS
KMS-12-PE MlXuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkjrTWM2OD1{Mj6yO|Qh|ryP M33uRnNCVkeHUh?=
NCI-H510A MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1;IbWlEPTB;MkSuNVI4QCEQvF2= NFXNSWtUSU6JRWK=
ES5 NXz4NYZ3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MojuTWM2OD1{ND63N|Q6KM7:TR?= NEL6O49USU6JRWK=
JiyoyeP-2003 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3;l[2lEPTB;Mk[uNlc1OiEQvF2= NGPKfmhUSU6JRWK=
NMC-G1 Ml\TS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MV\JR|UxRTJ5LkG4NlIh|ryP NVS3WJR1W0GQR1XS
NCI-H446 M3LmSGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYrJR|UxRTJ5LkS5OFYh|ryP MYTTRW5ITVJ?
NB7 NUTERmcyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmLRTWM2OD1{Nz65NlI6KM7:TR?= NFHzTlNUSU6JRWK=
A388 NHfRPYpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGHBZoVKSzVyPUK4MlAxPzRizszN M2fsVXNCVkeHUh?=
JVM-2 MmraS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoPKTWM2OD1{OD6yPFk5KM7:TR?= NV\zUnNiW0GQR1XS
HT-144 NWnTcVI6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3n5XmlEPTB;MkiuOlkh|ryP M2jKNnNCVkeHUh?=
NCI-H747 NXrrNoozT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkW2TWM2OD1{OD65NVk2KM7:TR?= MWfTRW5ITVJ?
NCI-H1650 NXrFO481T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnXhTWM2OD1{OT6wNVc3KM7:TR?= NUTnOGxsW0GQR1XS
EB-3 M3Pxfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlztTWM2OD1{OT61N|A6KM7:TR?= MmX0V2FPT0WU
KLE MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn3RTWM2OD1{OT62NVkh|ryP NF;MNldUSU6JRWK=
TK10 MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NI\MOZJKSzVyPUOwMlEzPiEQvF2= MYPTRW5ITVJ?
COLO-668 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlfYTWM2OD1|MD63PVIh|ryP MXzTRW5ITVJ?
NCI-H23 M3vHbGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmTBTWM2OD1|MT6xNFY{KM7:TR?= M2PUc3NCVkeHUh?=
GOTO M1SzbGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVrJR|UxRTNzLk[wPFUh|ryP NFvpN4lUSU6JRWK=
MSTO-211H NXTLNVF1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoDJTWM2OD1|MT64Olc5KM7:TR?= M4jzNnNCVkeHUh?=
LB831-BLC M37XUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYTJR|UxRTN{LkO4OFMh|ryP NEn2TGFUSU6JRWK=
SCH M1rNWmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{\2dWlEPTB;M{KuPFQ5PSEQvF2= MXXTRW5ITVJ?
EHEB NFvnbGhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYPvOm5sUUN3ME2zOE4yOTl|IN88US=> NXjTXVJYW0GQR1XS
U-266 MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkfiTWM2OD1|ND6yO|gyKM7:TR?= NGrlN|JUSU6JRWK=
EW-11 MkfiS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{HCeGlEPTB;M{SuOFczPSEQvF2= M2fLZ3NCVkeHUh?=
TE-9 NE\1TFZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYHqVFlYUUN3ME2zO{4xPDBzIN88US=> NXPOb4NLW0GQR1XS
ES3 NVTnVZhTT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoDuTWM2OD1|Nz61NFA1KM7:TR?= M1:0PHNCVkeHUh?=
NCI-H2141 MmTXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2Lz[WlEPTB;M{iuNFg1OyEQvF2= NHmwVFdUSU6JRWK=
MPP-89 NH3hdlZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUjKSplWUUN3ME20Nk4xPTh4IN88US=> M{O4U3NCVkeHUh?=
SK-MEL-2 NVXoPG5uT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{mweWlEPTB;NEKuOlQxPSEQvF2= MU\TRW5ITVJ?
LC-1F M3;rc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWHJR|UxRTR|LkO2PFIh|ryP Mo\IV2FPT0WU
NH-12 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3;KZ2lEPTB;NEOuPVM2QSEQvF2= MlroV2FPT0WU
RKO M{X6U2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3P4TmlEPTB;NESuNVI2OiEQvF2= NUHQ[JNwW0GQR1XS
KM-H2 NYP5[Gl2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mm\lTWM2OD12ND65OVc4KM7:TR?= M1qzVHNCVkeHUh?=
SK-UT-1 MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUjJR|UxRTR7Lki4NlUh|ryP M4HjTnNCVkeHUh?=

... Click to View More Cell Line Experimental Data

In vivo Consistent with the substantial and selective inhibition of VEGFR2 or PDGFR phosphorylation and signaling in vivo, Sunitinib (20-80 mg/kg/day) exhibits broad and potent dose-dependent anti-tumor activity against a variety of tumor xenograft models including HT-29, A431, Colo205, H-460, SF763T, C6, A375, or MDA-MB-435. Sunitinib dosing at 80 mg/kg/day for 21 days leads to complete tumor regression in six of eight mice, without tumor re-growing during a 110-day observation period after the end of treatment. Second round of treatment with Sunitinib remains efficacious against tumors that are not fully regressed during the first round of treatment. Sunitinib treatment results in significant decrease in tumor MVD, with ~40% reduction in SF763T glioma tumors. SU11248 treatment results in a complete inhibition of additional tumor growth of luciferase-expressing PC-3M xenografts, despite no reduction in tumor size. [2] Sunitinib treatment (20 mg/kg/day) dramatically suppresses the growth subcutaneous MV4;11 (FLT3-ITD) xenografts and prolongs survival in the FLT3-ITD bone marrow engraftment model. [3]

Protocol

Kinase Assay:[1]
+ Expand

Biochemical Tyrosine Kinase Assays:

IC50 values for Sunitinib against VEGFR2 (Flk-1) and PDGFRβ are determined using glutathione S-transferasefusion proteins containing the complete cytoplasmic domain of the RTK. Biochemical tyrosine kinase assays to quantitate the trans-phosphorylation activity of VEGFR2 (Flk-1) and PDGFRβ are performed in 96-well microtiter plates precoated (20 μg/well in PBS; incubated overnight at 4 °C) with the peptide substrate poly-Glu,Tyr (4:1). Excess protein binding sites are blocked with the addition of 1-5% (w/v) BSA in PBS. Purified GST-fusion proteins are produced in baculovirus-infected insect cells. GST-VEGFR2 and GST-PDGFRβ are then added to the microtiter wells in 2 × concentration kinase dilution buffer consisting of 100 mM HEPES, 50 mM NaCl, 40 μM NaVO4, and 0.02% (w/v) BSA. The final enzyme concentration for GST-VEGFR2 or GST-PDGFRβ is 50 ng/mL. Twenty-five μL of diluted Sunitinib are subsequently added to each reaction well to produce a range of inhibitor concentrations appropriate for each enzyme. The kinase reaction is initiated by the addition of different concentrations of ATP in a solution of MnCl2 so that the final ATP concentrations spanned the Km for the enzyme, and the final concentration of MnCl2 is 10 mM. The plates are incubated for 5-15 minutes at room temperature before stopping the reaction with the addition of EDTA. The plates are then washed three times with TBST. Rabbit polyclonal antiphosphotyrosine antisera are added to the wells at a 1:10,000 dilution in TBST containing 0.5% (w/v) BSA, 0.025% (w/v) nonfat dry milk, and 100 μM NaVO4 and incubated for 1 hour at 37 °C. The plates are then washed three times with TBST, followed by the addition of goat antirabbit antisera conjugated with horseradish peroxidase (1:10,000 dilution in TBST). The plates are incubated for 1 hour at 37 °C and then washed three times with TBST. The amount of phosphotyrosine in each well is quantitated after the addition of 2,2′-azino-di-[3-ethylbenzthiazoline sulfonate] as substrate.
Cell Research:[3]
+ Expand
  • Cell lines: RS4;11, MV4;11, and OC1-AML5
  • Concentrations: Dissolved in DMSO, final concentrations ~10 μM
  • Incubation Time: 24 and 48 hours
  • Method: Cells are starved overnight in medium containing 0.1% FBS prior to addition of Sunitinib and FL (50 ng/mL; FLT3-WT cells only). Proliferation is measured after 48 hours of culture using the Alamar Blue assay or trypan blue cell viability assays. Apoptosis is measured 24 hours after Sunitinib addition by Western blotting to detect cleavage of poly (ADP-ribose) polymerase (PARP) or levels of caspase-3.
    (Only for Reference)
Animal Research:[2]
+ Expand
  • Animal Models: Female nu/nu mice implanted s.c. with HT-29, A431, Colo205, H-460, SF763T, C6, A375, or MDA-MB-435, and male nu/nu mice bearing luciferase-expressing PC-3M tumors
  • Formulation: Formulated as a carboxymethyl cellulose suspension or as a citrate buffered (pH 3.5) solution
  • Dosages: ~80 mg/kg
  • Administration: Orally once daily
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 15 mg/mL (28.16 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents individually and in order:
4% DMSO+30% PEG 300+ddH2O
2mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 532.56
Formula

C22H27FN4O2.C4H6O5

CAS No. 341031-54-7
Storage powder
in solvent
Synonyms N/A

Bio Calculators

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Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

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*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).

Dilution Calculator

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Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02761057 Recruiting Recurrent Renal Cell Carcinoma|Stage III Renal Cell Cancer|Stage IV Renal Cell Cancer|Type 1 Papillary Renal Cell Carcinoma|Type 2 Papillary Renal Cell Carcinoma National Cancer Institute (NCI) April 2016 Phase 2
NCT02779283 Recruiting Untreated Adult Acute Myeloid Leukemia OHSU Knight Cancer Institute|National Cancer Institute (NCI) December 2015 Phase 1
NCT02626754 Enrolling by invitation Renal Cell Carcinoma vghtpe user|Taipei Veterans General Hospital, Taiwan August 2015 Phase 2
NCT02465060 Recruiting Advanced Malignant Neoplasm|Lymphoma|Recurrent Plasma Cell Myeloma|Recurrent Solid Neoplasm|Refractory Malignant Neoplasm|Refractory Plasma Cell Myeloma National Cancer Institute (NCI) August 2015 Phase 2
NCT01835158 Active, not recruiting Clear Cell Renal Cell Carcinoma|Metastatic Renal Cell Cancer|Stage III Renal Cell Cancer|Stage IV Renal Cell Cancer National Cancer Institute (NCI) July 2013 Phase 2
NCT01740154 Terminated Fatigue|Recurrent Renal Cell Cancer|Stage IV Renal Cell Cancer Case Comprehensive Cancer Center|National Cancer Institute (NCI) September 2012 --

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

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Frequently Asked Questions

  • Question 1:

    I was wondering that the compound is in its cis or trans form?

  • Answer:

    S1042 Sunitinib Malate is Z form.

  • Question 2:

    What is the difference between Sunitinib Malate(S1042) and Sunitinib(S7781)?

  • Answer:

    S1042 is the Malate salt form of Sunitinib. The biological activities of these two compounds are the same but the solubility of these two compounds in aqueous solvent are different.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID